Brimonidine's neuroprotective effects against transient ischaemia-induced retinal ganglion cell death

Citation
M. Vidal-sanz et al., Brimonidine's neuroprotective effects against transient ischaemia-induced retinal ganglion cell death, EUR J OPTHA, 11, 2001, pp. S36-S40
Citations number
31
Categorie Soggetti
Optalmology
Journal title
EUROPEAN JOURNAL OF OPHTHALMOLOGY
ISSN journal
11206721 → ACNP
Volume
11
Year of publication
2001
Supplement
2
Pages
S36 - S40
Database
ISI
SICI code
1120-6721(200107/09)11:<S36:BNEATI>2.0.ZU;2-Z
Abstract
PURPOSE. Brimonidine is a lowering pressure agent currently used in glaucom a. This chronic degenerative condition is characterised by neuronal death, and an agent which offers neuroprotection may slow down or impede the progr ession of neuronal cell death. METHODS. The effects of brimonidine (BMD) on the short- and long-term survi val of retinal ganglion cells (RGCs) after transient retinal ischaemia are reported here using a rat model. The fluorescent tracer Fluorogold (FG) was applied to both superior colliculi to retrogradely label RGCs. A ninety-mi nute period of ischaemia was induced and densities of surviving RGCs were e stimated over time by counting FG-labelled RGCs in 12 standard regions of e ach retina. RESULTS. Seven days after inducing transient ischaemia, there was loss of a pproximately half of the RGC population. Topical pre-treatment with 0.1 % o r 0.5% BMD prevented ischaemia-induced RGC death. CONCLUSIONS. These results indicate that optimal neuroprotective effects ag ainst the early loss of RGCs are seen with 0.1 % or 0.5% BMD. Ischaemia-ind uced RGC loss continued between day 7 and day 21 in the vehicle treated gro ups and amounted to approximately 25% of the RGC population. Topical pre-tr eatment with 0.1 % or 0.5% BMD was also effective in reducing the slow loss of RGCs.